ABSTRACT
This paper is addressed to presenting evidence that the basal ganglia are involved in mediating schizophrenia. Data from the experimental and clinical literature suggest a basal ganglionic role in higher cognitive processes, affect, and attention. Deficits of these same factors serve to characterize the major symptoms of schizophrenia. Moreover, psychiatric patients tend to have frank motor problems characteristic of basal ganglia lesions and pathological conditions of the basal ganglia manifest psychiatric difficulties as a major symptom. Taken together, these data are in accord with the hypothesis that some dysfunction involving the basal ganglia is a major factor in schizophrenia.
Subject(s)
Basal Ganglia/physiopathology , Schizophrenia/physiopathology , Affect/physiology , Attention/physiology , Basal Ganglia Diseases/physiopathology , Cognition/physiology , Dopamine/metabolism , Extrapyramidal Tracts/physiopathology , Humans , Limbic System/physiopathology , Motor Activity/physiology , Receptors, Dopamine/metabolism , Schizophrenic Psychology , Stereotyped Behavior/physiologyABSTRACT
Because considerable work has implicated the basal ganglia in oral-ingestive behavior, an assessment was made of the effects of trigeminal stimuli upon entopeduncular single units. Units wre recorded extracellularly in awake, paralyzed and locally anesthetized cats. The effects of two types of sensory input were tested. Afferents from periodontal mechano-receptors involved in reflex jaw opening were stimulated via electrodes in the inferior dental nerve. Afferents from stretch receptors involved in reflex jaw closure were stimulated via electrodes in the trigeminal mesencephalic nucleus. A significant proportion of cells responded to both types of stimulation. The data were discussed in the context of a basal ganglionic role in oropharyngeal motor processes and a more general role in movement per se.
